2016
DOI: 10.1016/j.ejphar.2015.12.024
|View full text |Cite
|
Sign up to set email alerts
|

Oxidative activation of CaMKIIδ in acute myocardial ischemia/reperfusion injury: A role of angiotensin AT1 receptor-NOX2 signaling axis

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1

Citation Types

2
12
0
1

Year Published

2016
2016
2023
2023

Publication Types

Select...
8
1

Relationship

1
8

Authors

Journals

citations
Cited by 17 publications
(15 citation statements)
references
References 49 publications
2
12
0
1
Order By: Relevance
“…In the current study, reinforcing the role of AT1 receptors in inflammatory condition, we demonstrated that Olme prevented the lipid peroxidation, as evidenced by MDA assay, associated with increased GSH levels and SOD enzyme activities, when compared with the untreated group. These results indicate that AT1 receptor blockade decreases the oxidative stress, consistent with prior findings …”
Section: Discussionsupporting
confidence: 92%
“…In the current study, reinforcing the role of AT1 receptors in inflammatory condition, we demonstrated that Olme prevented the lipid peroxidation, as evidenced by MDA assay, associated with increased GSH levels and SOD enzyme activities, when compared with the untreated group. These results indicate that AT1 receptor blockade decreases the oxidative stress, consistent with prior findings …”
Section: Discussionsupporting
confidence: 92%
“… Content of particular proteins indicating cellular injury due to apoptosis and necrosis has been investigated in ischemic/reperfused (IR) hearts and ischemic/reperfused hearts treated with CaMKII inhibitor and/or AT 1 receptor inhibitor. This data article provides information in support of the original research article “Oxidative activation of CaMKIIδ in acute myocardial ischemia/reperfusion injury: a role of angiotensin AT 1 receptor-NOX2 signaling axis” [1] . …”
supporting
confidence: 60%
“…This is an important finding of the study, which shows that the apelin‐13 induced protection is associated with decrease in AT1R expression. It has been reported that AT1R expression is increased rapidly after cardiac ischaemia and plays a critical role in the development of MI . This beneficial effect of apelin in the reduction of infarct size and improvement of myocardial contractility was inhibited by F13A (Figures and ).…”
Section: Discussionmentioning
confidence: 86%